A Model Based on Noninvasive Markers Predicts Very Low Hepatocellular Carcinoma Risk After Viral Response in Hepatitis C Virus-Advanced Fibrosis
A Model Based on Noninvasive Markers Predicts Very Low Hepatocellular Carcinoma Risk After Viral Response in Hepatitis C Virus-Advanced Fibrosis
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DOI：
10.1002/hep.31588
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发表时间：
2020-11-10
期刊：
影响因子：
13.5
通讯作者：
Banares, Rafael
中科院分区：
文献类型：
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作者：
Alonso Lopez, Sonia;Manzano, Maria Luisa;Banares, Rafael
背景和目的丙型肝炎病毒(丙型肝炎病毒)合并晚期纤维化的患者在持续病毒应答(SVR)后仍有患肝细胞癌(HCC)的风险，需要终身监测。由于肝细胞癌的风险不是均匀的，而且随着肝纤维化的消退而降低，我们的目的是基于对非侵入性标记物的预测及其在SVR后的变化来识别低风险的肝细胞癌患者。方法与结果这是一项多中心队列研究，包括经直接抗病毒药物治疗后达到SVR的丙型肝炎和代偿性晚期纤维化患者。记录治疗前、治疗结束后1年和3年的临床和瞬时弹性成像(TE)数据。所有患者每6个月进行一次肝脏超声检查。EOT后1年进行临床评估的患者符合条件。进行单因素和多因素COX回归分析，建立预测模型。采用Kaplan-Meier法评估肝细胞癌发生率。符合条件的患者993例(男性56%；女性44%；中位年龄62岁)，35例(3.9%)发展为肝癌，中位随访时间为45个月(范围13-53个月)。基线肝硬化值(HR 1.040；95%CI 1.017~1.064)、血清白蛋白(HR 0.400；95%CI 0.174~0.923)、1年DeltaLSM(HR 0.993；95%CI 0.987~0.998)、1年FIB4评分(HR 1.095；95%CI 1.046~1.146)是肝细胞癌的独立危险因素。基于TE的肝癌风险模型预测，在评分为0的患者(基线LSM4.2g/dL和1年DeltaLSM>；25.5%)的3年内，肝癌发生率为0%，而在评分为1-3的患者中，预测为5.2%(哈瑞尔的C 0.779；LOG-RANK 0.002)。与FIB-4类似的预测肝癌风险的替代模型。结论结合非侵入性标记物的基线和动态变化，可能有助于识别SVR后发生肝癌风险非常低的患者。
Background and Aims Patients with hepatitis C virus (HCV) and advanced fibrosis remain at risk of hepatocellular carcinoma (HCC) after sustained viral response (SVR) and need lifelong surveillance. Because HCC risk is not homogenous and may decrease with fibrosis regression, we aimed to identify patients with low HCC risk based on the prediction of noninvasive markers and its changes after SVR.Approach and Results This is a multicenter cohort study, including patients with HCV and compensated advanced fibrosis that achieved SVR after direct antivirals. Clinical and transient elastography (TE) data were registered at baseline, 1 year, and 3 years after the end of treatment (EOT). All patients underwent liver ultrasound scan every 6 months. Patients with clinical evaluation 1 year after EOT were eligible. Univariate and multivariate Cox regression analysis were performed, and predictive models were constructed. HCC occurrence rates were evaluated by Kaplan-Meier. Nine hundred and ninety-three patients were eligible (56% male; 44% female; median age 62 years), 35 developed HCC (3.9%), and the median follow-up was 45 months (range 13-53). Baseline liver stiffness measurement (LSM) (HR 1.040; 95% CI 1.017-1.064), serum albumin (HR 0.400; 95% CI 0.174-0.923), 1-year DeltaLSM (HR 0.993; 95% CI 0.987-0.998), and 1-year FIB-4 score (HR 1.095; 95% CI 1.046-1.146) were independent factors associated with HCC. The TE-based HCC risk model predicted 0% of HCC occurrence at 3 years in patients with score 0 (baseline LSM 4.2 g/dL, and 1-year DeltaLSM > 25.5%) versus 5.2% in patients with score 1-3 (Harrell's C 0.779; log-rank 0.002). An alternative model with FIB-4 similarly predicted HCC risk.Conclusions A combination of baseline and dynamic changes in noninvasive markers may help to identify patients with a very low risk of HCC development after SVR.